To date, numerous mechanisms have been identified in which one cell engulfs another, resulting in the creation of ‘cell-in-cell’ (CIC) structures, which subsequently cause cell death. One of the mechanisms of formation of these structures is entosis, which is presumably associated with possible carcinogenesis and tumour progression. The peculiarity of the process is that entotic cells themselves actively invade the host cell, and afterwards have several possible variants of fate. Entotic formations are structures where one cell is engulfed by another cell, creating a cell-in-cell structure. The nucleus of the outer cell has a crescent shape, while the inner cell is surrounded by a large entotic vacuole. These characteristics differentiate entosis from cell cannibalism. It’s worth noting that entotic formations are not necessarily harmful and may even be beneficial in some cases. In this article we will consider the mechanism of entosis and variants of entotic cell death, and also put forward hypothesis about possible variants of participation of this process on the formation and progression of cancer. This article also presents our proposed classification of functional forms of entosis.

One of the important reasons for the ineffectiveness of chemotherapy in breast cancer (BC) is considered to be the formation of a multidrug resistance phenotype in tumour cells, which is caused by the expression of energy-dependent ABC transporters. The aim of this work was to assess chromosomal aberrations and the level of transcripts of all 49 known ABC transporter genes in breast tumours. Materials and Methods. The study included 129 patients with breast cancer. A microarray study of all tumour samples was carried out on microchips. Results. This study established that the presence of a deletion in genes ABCB1, ABCB4, ABCB8, ABCC7, ABCC11, ABCC12, ABCF2, and ABCG4 is associated with an objective response to treatment (p ≤ 0.05). A decrease in the expression of genes was associated with a good response to chemotherapy, whereas an increase in expression caused the progression and stabilization of the tumour. Analysis of metastatic-free survival rates showed that the presence of ABCB1/4 and ABCC1/6 deletions was associated with 100% survival (log-rank test p = 0.01 and p = 0.03). Conclusions. The study showed that the aberrant state of ABC transporter genes, as well as a decrease in the expression of these genes, is a predictor of the effectiveness of therapeutic treatment and a potential prognostic marker of metastatic survival.

Increasingly, many researchers are focusing on the sensitivity in breast tumors (BC) to certain chemotherapy drugs and have personalized their research based on the assessment of this sensitivity. One such personalized approach is to assess the chemotherapy’s gene expression, as well as aberrations in the number of DNA copies—deletions and amplifications with the ability to have a significant effect on the gene’s activity. Thus, the aim of this work was to study the predictive and prognostic significance of the expression and chromosomal aberrations of eight chemosensitivity genes in breast cancer patients. Material and methods. The study involved 97 patients with luminal B breast cancer IIB–IIIB stages. DNA and RNA were isolated from samples of tumor tissue before and after treatment. Microarray analysis was performed for all samples on high-density microarrays (DNA chips) of Affymetrix (USA) CytoScanTM HD Array and Clariom™ S Assay, human. Detection of expression level of seven chemosensitivity genes—RRM1, ERCC1, TOP1, TOP2a, TUBB3, TYMS, and GSTP1—was performed using PCR real-time (RT-qPCR). Results. The expression of the RRM1 (AC scheme), TOP2α, TYMS, and TUBB3 genes in patients with an objective response to treatment (complete and partial regression) is higher than in patients with stabilization and progression (p < 0.05). According to our results, the presence of a high level of GSTP1 in a tumor biopsy is associated with the low efficiency of the NAC CP scheme (p = 0.05). The presence of RRM1 deletion is associated with complete and partial regression, as for the TOP1 and TUBB3 genes (p < 0.05). Higher rates of metastatic survival are associated with a high level of expression and amplification of the GSTP1 gene (log-rank test p = 0.02 and p = 0.05). Conclusion. Thus, a complex assessment of the chemotherapy’s gene expression is important not only for understanding the heterogeneity and molecular biology of breast cancer but also to obtain a more accurate disease prognosis.

Background: the present study aims to prove or disprove the hypothesis that the state of copy number aberration (CNA) activation of WNT signalling pathway genes accounts for the ability of differentiated tumour cells to emerge from postchemotherapy shock. Methods: In the first step, the CNA genetic landscape of breast cancer cell lines BT-474, BT-549, MDA-MB-231, MDA-MD-468, MCF7, SK-BR-3 and T47D, which were obtained from ATCC, was examined to rank cell cultures according to the degree of ectopic activation of the WNT signalling pathway. Then two lines of T47D with ectopic activation and BT-474 without activation were selected. The differentiated EpCAM+CD44-CD24-/+ cells of these lines were subjected to IL6 de-differentiation with formation of mammospheres on the background of cisplatin and WNT signalling inhibitor ICG-001. Results: it was found that T47D cells with ectopic WNT signalling activation after cisplatin exposure were dedifferentiated to form mammospheres while BT-474 cells without ectopic WNT-signalling activation did not form mammospheres. The dedifferentiation of T47D cells after cisplatin exposure was completely suppressed by the WNT signalling inhibitor ICG-001. Separately, ICG-001 reduced, but did not abolish, the ability to dedifferentiate in both cell lines. Conclusions: these data support the hypothesis that the emergence of differentiated tumour cells from postchemotherapy shock after chemotherapy is due to ectopic activation of WNT signalling pathway genes.

Background. One of the main reasons of the ineffectiveness of chemotherapy is still considered to be the formation of the multidrug resistance phenotype of the tumor due to the expression of energy-dependent proteins of ABC transporters. Our previous studies for some ABC genes have established that the expression of these genes correlates with the effectiveness of neoadjuvant chemotherapy (NAC). Some of the clinical studies indicate that ABC transporters can influence not only the formation of chemoresistance in the tumor, but also the progression, invasion and metastasis of the tumor node. Objective: to evaluate the level of transcription of all 49 known ABC genes in a breast tumor before and after treatment and their prognostic significance. Materials and methods. The study included 31 patients with a diagnosis of stage IIA – IIIB breast cancer. RNA was isolated from paired samples of tumor tissue before and after NAC. A microarray study of all tumor samples was performed on ClariomТМ S Assay, human microarrays. Using microarray studies, the expression of 49 genes of the ABC transporter family was studied. Analysis of the microchip data was carried out using the program Transcriptome Analysis Console (TAC) software 4.0. Results. It was found that changes in the expression (increase/decrease during NAC) of the ABCA5, ABCA7, ABCB1, ABCB4, ABCB11, ABCC1, ABCC10, ABCC11, ABCG1, ABCG2, ABCG4, ABCG5, ABCG8 genes are statistically significantly associated with the response to NAC. In addition, the prognostic significance of ABCB1 and ABCB4 gene expression was established. Survival analysis showed that 5-year survival rates in patients with high gene expression of ABCB1 and ABCB4 are lower compared to patients with low expression of these genes (log-rank-test p = 0.001 and 0.04 respectively). Conclusion. Data were obtained on the relationship of gene expression of the ABC transporter family with the effect of NAC in patients with breast cancer and the outcome of the disease. The prognostic potential of the ABCB1 and ABCB4 genes in patients with breast cancer has been established.

Введение. Этиология рака полового члена (РПЧ) является многофакторной, в частности, интересным вопросом является ассоциация инфицирования вирусом папилломы человека (ВПЧ) с риском развития рака полового члена. Имеющиеся в литературе результаты по выявлению ВПЧ при новообразованиях полового члена очень противоречивы по сравнению с аналогичными при других ВПЧ-ассоциированных онкопатологиях. Цель исследования. Систематизация имеющихся мировых литературных данных относительно связи наличия ВПЧ-инфекции с риском возникновения рака полового члена. Материалы и методы. Поиск проводился с помощью баз данных Pubmed, NCBI и поискового сервиса Google scholar. В результате литературного поиска первично было получено 205 статей по изучаемой тематике, опубликованных с 1991 по 2020 гг. В окончательный анализ вошли 9 исследований, соответствующие абсолютно всем заданным параметрам. Результаты. Показано, что ВПЧ определяется почти в равной степени как при доброкачественных образованиях и предраковых поражениях полового члена, так и среди образцов нормальной ткани полового члена (контрольных групп). В то время как имеется значительное отличие в количестве ВПЧ-положительных пациентов среди больных с диагнозом рак полового члена и контрольной группой, OR = 142,6. Также определено, что самыми распространёнными генотипами ВПЧ высокого канцерогенного риска (ВКР) оказались 16 и 18. Заключение. Результаты систематического обзора подтвердили высокую степень риска возникновения РПЧ при наличии ВПЧ инфекции, а также высокий уровень инфицированности ВПЧ при РПЧ (62,0 %).